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| Author’s name/study name | Outcome | Gene (variant) | Sample size/drug | Effect estimates and findings |
|
| Hindorff et al. [22] | Nonfatal MI/nonfatal stroke | ABCB1, CETP, HMGCR, LDLR, LIPC, NOS3 | 865 with MI, 368 with stroke and 2686 controls/statins | No gene-statin interactions for stroke.
5 SNP-statin interactions on stroke (one CETP, four LIPC); no gene level association for stroke; SNP level association: two SNPs (one CETP, one LDLR) for stroke.
The highest significance was found for stroke in CETP rs5883 carriers on simvastatin (OR 3.60 95% CI 1.22–7.70) |
|
| Heart protection study [23] | Major coronary event (coronary death or nonfatal MI), major vascular event (major coronary event plus revascularization or stroke) | KIF6 Trp719Arg polymorphism (rs20455) on vascular risk and response to statin therapy in from of the heart protection study | 18,348 participants/simvastatin | No significant gene-statin interaction with any of the outcome, including stroke |
|
| Rotterdam study [24] | Death, MI, stroke | Apo E (E2, E3, E4) | 7983 older than 55 yo/statins | No significant gene-statin interaction with any of the outcome.
Statins reduce stroke risk (aOR 0.50 95% CI 0.28–0.91) independently of Apo E genotype |
|
| GenHAT [25] | Primary outcome: all-cause mortality, secondary outcomes (fatal CHD and nonfatal MI, CVD mortality, CHD, stroke, other CVD, non-CVD mortality, stroke, and heart failure) | ACE (I/D) | 9467/pravastatin | No significant gene-statin interaction with any of the outcome |
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